Peri/Epicellular Protein Disulfide Isomerase Sustains Vascular Lumen Caliber Through an Anticonstrictive Remodeling Effect

dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorTANAKA, Leonardo Y.
dc.contributor.authorARAUJO, Haniel A.
dc.contributor.authorHIRONAKA, Gustavo K.
dc.contributor.authorARAUJO, Thais L. S.
dc.contributor.authorTAKIMURA, Celso K.
dc.contributor.authorRODRIGUEZ, Andres I.
dc.contributor.authorCASAGRANDE, Annelise S.
dc.contributor.authorGUTIERREZ, Paulo S.
dc.contributor.authorLEMOS-NETO, Pedro Alves
dc.contributor.authorLAURINDO, Francisco R. M.
dc.date.accessioned2016-03-14T14:32:19Z
dc.date.available2016-03-14T14:32:19Z
dc.date.issued2016
dc.description.abstractWhole-vessel remodeling critically determines lumen caliber in vascular (patho)physiology, and it is reportedly redox-dependent. We hypothesized that the cell-surface pool of the endoplasmic reticulum redox chaperone protein disulfide isomerase-A1 (peri/epicellular=pecPDI), which is known to support thrombosis, also regulates disease-associated vascular architecture. In human coronary atheromas, PDI expression inversely correlated with constrictive remodeling and plaque stability. In a rabbit iliac artery overdistension model, there was unusually high PDI upregulation (approximate to 25-fold versus basal, 14 days postinjury), involving both intracellular and pecPDI. PecPDI neutralization with distinct anti-PDI antibodies did not enhance endoplasmic reticulum stress or apoptosis. In vivo pecPDI neutralization with PDI antibody-containing perivascular gel from days 12 to 14 post injury promoted 25% decrease in the maximally dilated arteriographic vascular caliber. There was corresponding whole-vessel circumference loss using optical coherence tomography without change in neointima, which indicates constrictive remodeling. This was accompanied by decreased hydrogen peroxide generation. Constrictive remodeling was corroborated by marked changes in collagen organization, that is, switching from circumferential to radial fiber orientation and to a more rigid fiber type. The cytoskeleton architecture was also disrupted; there was a loss of stress fiber coherent organization and a switch from thin to medium thickness actin fibers, all leading to impaired viscoelastic ductility. Total and PDI-associated expressions of 1-integrin, and levels of reduced cell-surface 1-integrin, were diminished after PDI antibody treatment, implicating 1-integrin as a likely pecPDI target during vessel repair. Indeed, focal adhesion kinase phosphorylation, a downstream 1-integrin effector, was decreased by PDI antibody. Thus, the upregulated pecPDI pool tunes matrix/cytoskeleton reshaping to counteract inward remodeling in vascular pathophysiology.
dc.description.indexMEDLINE
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [09/54764-6, 09/51654-5, 10/06360-0, 13/06241-0]
dc.description.sponsorshipCentro de Pesquisa
dc.description.sponsorshipCentro de Pesquisa, Inovacao e Difusao FAPESP (CEPID Processos Redox em Biomedicina) [13/07937-8]
dc.description.sponsorshipInstituto Nacional de Ciencia, Tecnologia e Inovacao de Processos Redox em BioMedicina (INCTRedoxoma, CNPq)
dc.description.sponsorshipFundacao Zerbini
dc.identifier.citationHYPERTENSION, v.67, n.3, p.613-622, 2016
dc.identifier.doi10.1161/HYPERTENSIONAHA.115.06177
dc.identifier.eissn1524-4563
dc.identifier.issn0194-911X
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/13587
dc.language.isoeng
dc.publisherLIPPINCOTT WILLIAMS & WILKINS
dc.relation.ispartofHypertension
dc.rightsrestrictedAccess
dc.rights.holderCopyright LIPPINCOTT WILLIAMS & WILKINS
dc.subjectcytoskeleton
dc.subjectendoplasmic reticulum
dc.subjecthydrogen peroxide
dc.subjectprotein disulfide isomerase
dc.subjectvascular remodeling
dc.subject.otheraortic-aneurysm formation
dc.subject.otherthrombus formation
dc.subject.otherendothelial-cells
dc.subject.otherthiol isomerases
dc.subject.otherblood-flow
dc.subject.otherredox
dc.subject.othermice
dc.subject.otherangioplasty
dc.subject.otheractivation
dc.subject.otherrestenosis
dc.subject.wosPeripheral Vascular Disease
dc.titlePeri/Epicellular Protein Disulfide Isomerase Sustains Vascular Lumen Caliber Through an Anticonstrictive Remodeling Effect
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.author.externalRODRIGUEZ, Andres I.:Univ Sao Paulo, Sch Med, Vasc Biol Lab, Heart Inst InCor, Ave Eneas C Aguiar,44,Annex 2,9th Floor, BR-05403000 Sao Paulo, Brazil
hcfmusp.author.externalCASAGRANDE, Annelise S.:Univ Sao Paulo, Sch Med, Vasc Biol Lab, Heart Inst InCor, Ave Eneas C Aguiar,44,Annex 2,9th Floor, BR-05403000 Sao Paulo, Brazil
hcfmusp.citation.scopus34
hcfmusp.contributor.author-fmusphcLEONARDO YUJI TANAKA
hcfmusp.contributor.author-fmusphcHANIEL ALVES ARAUJO
hcfmusp.contributor.author-fmusphcGUSTAVO KEN HIRONAKA
hcfmusp.contributor.author-fmusphcTHAIS LARISSA ARAUJO DE OLIVEIRA SILVA
hcfmusp.contributor.author-fmusphcCELSO KIYOCHI TAKIMURA
hcfmusp.contributor.author-fmusphcPAULO SAMPAIO GUTIERREZ
hcfmusp.contributor.author-fmusphcPEDRO ALVES LEMOS NETO
hcfmusp.contributor.author-fmusphcFRANCISCO RAFAEL MARTINS LAURINDO
hcfmusp.description.beginpage613
hcfmusp.description.endpage622
hcfmusp.description.issue3
hcfmusp.description.volume67
hcfmusp.origemWOS
hcfmusp.origem.pubmed26781284
hcfmusp.origem.scopus2-s2.0-84958063700
hcfmusp.origem.wosWOS:000369755200025
hcfmusp.publisher.cityPHILADELPHIA
hcfmusp.publisher.countryUSA
hcfmusp.relation.referenceEssex DW, 2009, ANTIOXID REDOX SIGN, V11, P1191, DOI 10.1089/ARS.2008.2322
hcfmusp.relation.referenceAzevedo LCP, 2000, CARDIOVASC RES, V47, P436, DOI 10.1016/S0008-6363(00)00091-2
hcfmusp.relation.referenceDeguchi JO, 2009, LAB INVEST, V89, P315, DOI 10.1038/labinvest.2008.167
hcfmusp.relation.referenceEble JA, 2014, ANTIOXID REDOX SIGN, V20, P1977, DOI 10.1089/ars.2013.5294
hcfmusp.relation.referenceEletto D, 2014, J CELL SCI, V127, P3649, DOI 10.1242/jcs.153643
hcfmusp.relation.referenceMulvany MJ, 2012, BASIC CLIN PHARMACOL, V110, P49, DOI 10.1111/j.1742-7843.2011.00758.x
hcfmusp.relation.referenceBi SG, 2011, P NATL ACAD SCI USA, V108, P10650, DOI 10.1073/pnas.1017954108
hcfmusp.relation.referenceWan SW, 2012, J CELL BIOCHEM, V113, P1681, DOI 10.1002/jcb.24037
hcfmusp.relation.referenceSAREMBOCK IJ, 1989, CIRCULATION, V80, P1029
hcfmusp.relation.referencePescatore LA, 2012, J BIOL CHEM, V287, P29290, DOI 10.1074/jbc.M112.394551
hcfmusp.relation.referenceRudic RD, 1998, J CLIN INVEST, V101, P731, DOI 10.1172/JCI1699
hcfmusp.relation.referenceBurgoyne JR, 2007, SCIENCE, V317, P1393, DOI 10.1126/science.1144318
hcfmusp.relation.referenceLehoux S, 2006, CARDIOVASC RES, V71, P269, DOI 10.1016/j.cardiores.2006.05.008
hcfmusp.relation.referenceCho J, 2008, J CLIN INVEST, V118, P1123, DOI 10.1172/JCI34134
hcfmusp.relation.referenceSchoenhagen P, 2006, CIRCULATION, V113, P2826, DOI 10.1161/CIRCULATIONAHA.105.585703
hcfmusp.relation.referenceCai H, 2001, ARTERIOSCL THROM VAS, V21, P1571, DOI 10.1161/hq1001.097028
hcfmusp.relation.referenceLaurindo FRM, 2012, FREE RADICAL BIO MED, V52, P1954, DOI 10.1016/j.freeradbiomed.2012.02.037
hcfmusp.relation.referenceLafont A, 1999, CIRCULATION, V100, P1109
hcfmusp.relation.referenceMuller C, 2013, ANTIOXID REDOX SIGN, V18, P731, DOI 10.1089/ars.2012.4577
hcfmusp.relation.referenceSwiatkowska M, 2010, J BIOL CHEM, V285, P29874, DOI 10.1074/jbc.M109.092486
hcfmusp.relation.referenceFurlan-Freguia C, 2011, J CLIN INVEST, V121, P2932, DOI 10.1172/JCI46129
hcfmusp.relation.referenceTian F, 2009, AM J PHYSIOL-HEART C, V297, pH1078, DOI 10.1152/ajpheart.00937.2008
hcfmusp.relation.referenceTaylor AJ, 1999, J AM COLL CARDIOL, V34, P760, DOI 10.1016/S0735-1097(99)00275-2
hcfmusp.relation.referenceFurie B, 2014, CIRC RES, V114, P1162, DOI 10.1161/CIRCRESAHA.114.301808
hcfmusp.relation.referenceWillems SH, 2010, BIOCHEM J, V428, P439, DOI 10.1042/BJ20100179
hcfmusp.relation.referenceLeite PF, 2003, ARTERIOSCL THROM VAS, V23, P2197, DOI 10.1161/01.ATV.0000093980.46838.41
hcfmusp.relation.referenceHatahet F, 2009, ANTIOXID REDOX SIGN, V11, P2807, DOI 10.1089/ARS.2009.2466
hcfmusp.relation.referenceStanic B, 2010, ARTERIOSCL THROM VAS, V30, P2234, DOI 10.1161/ATVBAHA.110.207639
hcfmusp.relation.referenceLANGILLE BL, 1986, SCIENCE, V231, P405, DOI 10.1126/science.3941904
hcfmusp.relation.referenceLaurindo FRM, 2014, ANTIOXID REDOX SIGN, V20, P2755, DOI 10.1089/ars.2013.5605
hcfmusp.relation.referenceSwiatkowska M, 2008, FEBS J, V275, P1813, DOI 10.1111/j.1742-4658.2008.06339.x
hcfmusp.relation.referencePasterkamp G, 2000, CARDIOVASC RES, V45, P843, DOI 10.1016/S0008-6363(99)00377-6
hcfmusp.relation.referenceKim K, 2013, BLOOD, V122, P1052, DOI 10.1182/blood-2013-03-492504
hcfmusp.relation.referenceHahm E, 2013, BLOOD, V121, P3789, DOI 10.1182/blood-2012-11-467985
hcfmusp.relation.referenceSobierajska K, 2014, J BIOL CHEM, V289, P5758, DOI 10.1074/jbc.M113.479477
hcfmusp.relation.referenceCote G, 1999, CIRCULATION, V99, P30
hcfmusp.relation.referenceMaiellaro-Rafferty K, 2011, AM J PHYSIOL-HEART C, V301, pH355, DOI 10.1152/ajpheart.00040.2011
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